cardiac muscles; the heart as a pump and function of valve Flashcards

1
Q

cardia rhythmicity

A

trasmiting action potentais through the cardiac muscles to cause the hearts rhythmical beat

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2
Q

three types of cardiac muscles

A
  1. atrial muscles
  2. ventricle muscles
  3. excitatory and conductive muscle fiber
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3
Q

how excitatory and conductive fibers contract?

A

the contract by automatic rhythmical electrical discharge in the form of action potential or conduction of action potential by the heart that creates an excitatory system that controls the systematic beating of the heart

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4
Q

Explain left ventricle rotation

A

the left ventricle twists during a systole . It has muscle fiber layers. The subepicardial (outer) layer spirals towards right and the subendocardial (inner) spirals towards the left which causes the apex of the heart to move clockwise and the base to move anticlockwise
During systole the ventricle moves downwards the apex and after systole it recoils untwist during relaxation diastole

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5
Q

Cardiac muscle is a syncytium

A

the cells if cardiac muscles are joined together by intercalated disks. These intercalated disk join the cardiomyocytes by making a permeable connection between the cells (gap junction). The ions move across this junction to neighbouring cells which also allows action potential to move across each cell. Cardiac muscle is a syncytium of many heart cells that are so interconnected that when one cell gets excited all the cells receives the action potential

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6
Q

two syncytia

A

atrial syncytia and ventricle syncytia

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7
Q

What separatees atrium and ventricle

A

fibrous tissue that surround the atrioventricular valve.

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8
Q

how action potential spreads from atria to ventrucle

A

by AV bundle

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9
Q

Action potential recorded in ventricle

A

stays about average of 105 millivolts. Intracellular potential goes from a negative between beats of -85 millivolt to positive of +20 millivolt. After spike the membrane remains depolarized for 0.2 secs, and repolarizes again.

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10
Q

Causes of long action potential in cardia muscles

A
  1. Contains slow calcium channels, which open late and then remain open for a tenth of a second intitiates the contraction.
  2. Immediately after the onset of a action potential the permeability of positive K ions decrease by five fold, which stops the efflux of +vely charged K ions during action potential and prevents early return of action potential to its normal level
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11
Q

Phase 0

A

Cardiac cell stimulated and depolarizes, making the action potential positive to 20millivolts. Voltage gated fast sodium channels open and Na efflux increases

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12
Q

Phase 1

A

initial repolarization- Na channels close and potassium leaves the cell

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13
Q

phase 2

A

initial repolarization occurs and then action potential plateaus causes of increase calcium permeability and decrease K permeability. The Ca channels open at phase 0 &1 and potassium channels close, which stops the efflux of K ions to the outside

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14
Q

Phase 3

A

opening of K channels causes efflux of K ions and closing of Ca channels and cello membrane return to normal action potential

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15
Q

Phase 4

A

resting membrane potential averages about -80to -90

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16
Q

Velocity if signal conduction in heqrt

A

0.3 to 0.5 m/sec which is 1/250 the velocity of a large nerve fiber and 1/10 of a skeletal muscle. 4m/sec in purkinjee fiber

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17
Q

refractory period ?

A

it is the interval of time in which the cardiac impulse cannot re excite an already excited cardiac muscle

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18
Q

Values of refractory period

A
  1. 25-0.30 second for ventricles

0. 15 for atrial

19
Q

Relative refractory period

A

Addition 0.05 second during which an excited muscle is more Hard to re-excite but it can still be re excited with a very strong excitation signal

20
Q

Explain the process of excitation that happens in same way in skeletal ma

A

he action potential reaches the the interior of cardiac muscles, from there jt travels to the membranes of longitudinal T tubules then it acts on the membrane of sarcoplasmic tubules which causes the release of calcium ions into the muscle sarcoplasm and in few thousandth of seconds actin and myosin filaments slide over each other to cause muscle contraction

21
Q

What differently happens in cardiac muscle than in skeletal muscle during muscle contraction

A

Calcium ions from T tubule also diffuse into the sarcoplasm, which opens the voltage dependant calcium channels in the membrane of T tubule, calcium entering the cell then activates calcium release channels or ryanodine receptors in the sarcoplasmic reticulum triggering the calcium ions to be released in the sarcoplasm

22
Q

Cardiac cycle

A

the events from the begging of one heartbeat to the begging of the other is called as cardiac cycle

23
Q

Explain where cardiac cycle in events

A

starts from sinus node which is present on the superior lateral wall of right atrium from where the superiors vena cave enters then passes to both atria then to Av bundle and then to ventricles.

24
Q

Why atria are prime pumpers

A

there is a delay of more than 0.1 second during the passage of each cardiac impulse from atria to ventricle . So the atria contracts ahead of ventricle

25
Q

Period of rapid filling of ventricle

A

During a ventricular systole, large amount of blood accumulate in right and left atrial due to closed AV valve. During ventricle diastole, the pressure inside the ventricles decreases and the already made pressure in the atria during ventricle systole causes the opening of AV Valve and rapidly fills the ventricle with blood

26
Q

The three thirds of diastole in which the blood fills the ventricle

A

in healthy humans the period of rapid filling of ventricle lasts for the first third of the diastole. The mid third is when a very small amount of blood passes to ventricles which the the blood coming from veins into the atria and it passes directly into the ventricle. The last third is when the atria contracts and give additional thurst and fills the heart with the 20% of blood to the heart

27
Q

What happens to people heart disease

A

In cardiac fibrosis or diabetes mellitus the ventricles stiffen up this causes less blood to fill the ventricles during the early diastoles and require more volume or more filling from later atrial contraction

28
Q

Period of isovolumic contraction

A

when the ventricle contracts, it takes 0.2 to 0.3 second to to build up sufficient pressure to push the semilunar valves. In this time contraction is occurring but no emptying is done that is the muscle tension is increasing but no muscle shortening is happening

29
Q

period of ejection

A

when the pressure of left ventricle increases more than 80 mm Hg the pressure opens the semilunar valves and the blood goes into the aorta and pulmonary artery. 60% of the blood is ejected at the end of the diastole, 70% is ejected in First third Called period of rapid ejection and the 30% is ejected in the rest of the two thirds called the period of slow ejection

30
Q

Period of isovolumic relaxation

A

at the end of systole, ventricle relaxation behinds and the pressure decreases in the ventricles. The aorta and pulmonary artery valves to be closed when the hood in send back because of pressure created in the distended arteries. 0.03 to 0.06 second is taken More by ventricle to relax, even though the volume isn’t changing

31
Q

End diastolic volume

A

When the blood enters the ventricle the increase In volume of each of the ventricle is 110 to 120 ml called as end diastolic volume

32
Q

Stroke volume output

A

when the ventricles get empty the volume decreases by about 70ml stroke volume output

33
Q

End systolic volume

A

remaining volume in each ventricles is 40 to 50ml called end systolic volume

34
Q

Ejection fraction

A

the fraction of end diastolic volume that is ejected is 60%. It is clinically used to asses cardiac systolic pumping

35
Q

where are papillary muscles in the heart are founds

A

they are attached to the vane of av valves by the chordae tendineae.

36
Q

Functions of papillary muscles in heart

A

They papillary muscles contract when the ventricle walls contract, they pull on vanes of the valve pulling them inwards into the ventricle preventing them from bulging too much into the atria

37
Q

preload

A

the degree of tension in the muscle when it becomes contracted is pre load

38
Q

after load

A

the load against which the muscles exerts the contractile force

39
Q

basic mechanisms of regulation of heart pumping

A
  1. intrinsic cardiac pumping regulation in response to the change in the volume of blood flow
  2. regulation of heart beat through the autonomic nervous system
40
Q

Frank sterling mechanism of the heart

A

the intrinsic ability of heart to manage blood flow is called Frank steeling mechanism of heart. It means the greater the heart muscle is stretched during blood filling, the greater the force of contraction, the greater the quantity of blood flown into aorta

41
Q

Effect of K ions on hear function

A

increased level of K ions in extracellular fluid makes the heart dilated and flaccid, also decreases the cardiac impulses travelling from atrial to ventricle through Av node. Only 2-3 times more value than normal of K ions can cause abnormal rhythm and death

42
Q

Why k ions have that affect

A

it lowers the membrane potential by causing depolarization, low membrane potential means Low action potential intensity and intensity muscle contraction weakens

43
Q

Effect of Ca ions

A

opposite effect to K ions, it causes spastic contractions